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Titolo:
Folate dependence of hyperhomocysteinemia and vascular dysfunction in cystathionine beta-synthase-deficient mice
Autore:
Lentz, SR; Erger, RA; Dayal, S; Maeda, N; Malinow, MR; Heistad, DD; Faraci, FM;
Indirizzi:
Univ Iowa, Coll Med, Dept Internal Med, Iowa City, IA 52242 USA Univ IowaIowa City IA USA 52242 pt Internal Med, Iowa City, IA 52242 USA Univ Iowa, Coll Med, Dept Pharmacol, Iowa City, IA 52242 USA Univ Iowa Iowa City IA USA 52242 Dept Pharmacol, Iowa City, IA 52242 USA Vet Affairs Med Ctr, Iowa City, IA 52246 USA Vet Affairs Med Ctr Iowa City IA USA 52246 d Ctr, Iowa City, IA 52246 USA Univ N Carolina, Dept Pathol, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 athol, Chapel Hill, NC 27599 USA Oregon Reg Primate Res Ctr, Beaverton, OR 97006 USA Oregon Reg Primate ResCtr Beaverton OR USA 97006 Beaverton, OR 97006 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 3, volume: 279, anno: 2000,
pagine: H970 - H975
SICI:
0363-6135(200009)279:3<H970:FDOHAV>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; PROTEIN-C ACTIVATION; ENDOTHELIAL DYSFUNCTION; ATHEROSCLEROTIC MONKEYS; CARDIOVASCULAR-DISEASE; ATHEROGENIC STIMULUS; PLASMA HOMOCYSTEINE; COFACTOR ACTIVITY; FOLIC-ACID; HYPERHOMOCYST(E)INEMIA;
Keywords:
acetylcholine; atherosclerosis; endothelium; homocysteine; thrombomodulin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Lentz, SR Univ Iowa, Coll Med, Dept Internal Med, C303 GH, Iowa City, IA 52242 USA Univ Iowa C303 GH Iowa City IA USA 52242 Iowa City, IA 52242 USA
Citazione:
S.R. Lentz et al., "Folate dependence of hyperhomocysteinemia and vascular dysfunction in cystathionine beta-synthase-deficient mice", AM J P-HEAR, 279(3), 2000, pp. H970-H975

Abstract

Hyperhomocysteinemia is a risk factor for stroke, myocardial infarction, and venous thrombosis. Moderate hyperhomocysteinemia is associated with impaired endothelial function, but the mechanisms responsible for endothelial dysfunction in hyperhomocysteinemia are poorly understood. We have used genetic and dietary approaches to produce hyperhomocysteinemia in mice. Heterozygous cystathionine beta-synthase-deficient mice (CBS +/-), which have a selective defect in homocysteine transsulfuration, and wildtype (CBS +/+) littermates were fed either a control diet or a diet that is relatively deficient in folic acid for 6 wk. Plasma total homocysteine was 5.3 +/- 0.7 mu M in CBS +/+ mice and 6.4 +/- 0.6 mu M in CBS +/- mice (P = 0.3) given the control diet. Plasma total homocysteine was 11.6 +/- 4.5 mu M in CBS +/+ miceand 25.1 +/- 3.2 mu M in CBS +/- mice (P = 0.004) given a low-folate diet. In mice fed the control diet, relaxation of aortic rings in response to the endothelium-dependent vasodilator acetylcholine did not differ significantly between CBS +/+ mice and CBS +/- mice. In contrast, in mice fed a low-folate diet, maximal relaxation to acetylcholine was markedly impaired in CBS +/- mice (58 +/- 9%) compared with CBS +/+ mice (84 +/- 4%) (P = 0.01). No differences in relaxation to the endothelium-independent vasodilator sodium nitroprusside were observed among the four groups of mice. These data indicate that CBS-deficient mice are predisposed to hyperhomocysteinemia during dietary folate deficiency, and moderate hyperhomocysteinemia is associated with marked impairment of endothelial function in mice.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 05:20:18